Neuroblastoma （NB）， the commonest extracranial solid malignant tumor in children， is an adrenergic-derived neuroendocrine tumor characterized by highly heterogeneous clinical manifestations. Children with high-risk NB exhibit poor prognosis， often experiencing recurrence or metastasis despite intensive intervention. NB cells primarily consist of two subtypes： adrenergic （ADRN） and mesenchymal （MES）. The ADRN subtype is associated with differentiation and demonstrates greater sensitivity to differentiation-inducing agents and chemotherapeutic drugs， whereas the MES subtype correlates with invasiveness and chemotherapy resistance. Studies indicate that lineage transition between ADRN and MES subtypes contributes to tumor heterogeneity， potentially triggering chemotherapy resistance or recurrence. Elucidating the molecular mechanisms underlying their interconversion is crucial for overcoming lineage-transition-induced drug resistance and targeting ADRN in high-risk NB treatment. This article comprehensively reviews the role of adrenergic signaling in NB pathogenesis and its intrinsic molecular regulatory mechanisms while summarizing recent advances in ADRN-targeted strategies for NB clinical diagnosis and treatment， with an aim to provide a theoretical basis for future clinical management and prevention of NB.

Chronic kidney disease （CKD） is a common disease with high morbidity and mortality. Increasing evidence has indicated that programmed cell death （PCD） plays a significant role in the pathogenesis and progression of CKD. Non-coding RNA （ncRNA）， defined as a category of RNA that lacks coding potential， has emerged as a pivotal regulator of gene expression. This regulatory function of ncRNA extends to various biological processes， including PCD. This paper reviews the recent advances on the involvement of ncRNAs in the regulation of apoptosis， autophagy， pyroptosis， ferroptosis， necroptosis， and PANoptosis in CKD. It explores the crosstalk between different pathways and categorizes therapeutic strategies targeting ncRNA regulation of PCD into three main areas： the active ingredients of traditional Chinese medicine， tissue engineering technologies， and drugs. The objective of this study is to identify novel therapeutic targets and strategies for clinical treatment.

Mitophagy is an evolutionarily highly conserved selective autophagy process that maintains cellular homeostasis and mitochondrial quality control by specifically recognizing and removing damaged or superfluous mitochondria. During tumorigenesis， mitophagy eliminates damaged mitochondria and reduces the accumulation of reactive oxygen species （ROS）， thereby helping to sustain cellular homeostasis. Energy metabolism refers to the core biological process through which cells convert chemical energy from nutrients into adenosine triphosphate （ATP） via biochemical pathways such as glycolysis and oxidative phosphorylation， providing energy for cellular activities. While research on gastrointestinal tumors is advancing rapidly， a major bottleneck lies in their complex metabolic adaptations and therapeutic resistance. Targeting the interplay between mitophagy and energy metabolism has emerged as a promising therapeutic strategy for this disease. Current research on mitophagy and energy metabolism in gastrointestinal tumors， including the molecular mechanisms of their bidirectional regulatory network and applications in targeted therapies， remains to be systematically elucidated. Therefore， this review summarizes the implications of the mitophagy-energy metabolism interplay in gastrointestinal tumors， with the aim of providing insights for future research.

Normal tension glaucoma （NTG） is recognized as a distinct subtype of primary open-angle glaucoma， characterized by normal intraocular pressure （IOP<21 mmHg） in conjunction with progressive optic neuropathy， retinal ganglion cell （RGC） apoptosis， and visual field defects. The pathogenesis of NTG is predominantly independent of IOP， with fundamental processes involving genetic and mitochondrial factors， including RGC degeneration， neuroinflammation， mitochondrial dysfunction， and genetic predisposition. This article systematically reviews the IOP-independent and gene-driven mechanisms underlying NTG， with a particular focus on the roles of OPTN， TBK1， FOXC1， and OPA1 in inducing RGC damage through pathways such as mitochondrial dysfunction， glial cell activation， inflammatory signaling， apoptosis， and axonal degeneration. Among these genes， OPTN and TBK1 collectively contribute to the development of NTG by disrupting autophagy-mitochondrial homeostasis， causing defects in axonal transport， and activating neuroinflammatory pathways. FOXC1 is implicated in the progression of RGC degeneration through transcriptional regulation， while mutations in OPA1 lead to mitochondria-dependent RGC apoptosis.Additionally， this article provides a comprehensive review of the epigenetic regulation of METTL23， mitochondrial DNA mutations， the role of Alcadein α in axonal transport， the correlation between genes associated with primary open-angle glaucoma （POAG） and normal-tension glaucoma （NTG）， as well as susceptibility loci identified through genome-wide association studies （GWAS）. In the realm of translational research， recent advancements in therapeutic studies encompass strategies such as targeting OPTN E50K， inhibiting CRMP2 phosphorylation， and employing gene augmentation， gene silencing， and gene editing techniques. The etiology of NTG is complex， predominantly independent of intraocular pressure （IOP）， and arises from the interplay between genetic and environmental factors. This article seeks to promote mechanism-based technological innovation， optimize neuroprotective strategies for NTG， and enhance clinical translation， ultimately aiming to achieve precise treatment and improve visual function outcomes for patients.

Ischemic stroke （IS） is a cerebrovascular disease caused by thrombosis or embolism that interrupts cerebral blood flow， resulting in brain tissue damage. Mitochondria serve as the primary site for energy metabolism and are also involved in key biological processes， including calcium signal regulation， reactive oxygen species generation， and apoptosis initiation. Therefore， the structural and functional integrity of mitochondrial is crucial for neuronal survival， and the mitochondrial quality control （MQC） system is fundamental for maintaining mitochondrial homeostasis. The MQC system maintains mitochondrial network homeostasis by synergistically regulating key processes such as biogenesis， dynamics balance （fusion and fission）， autophagy， oxidative stress clearance， and calcium homeostasis. However， following IS， neurons undergo pathological changes-including inflammatory responses， oxidative stress， and excitatory amino acid toxicity- due to ischemia and hypoxia. These factors collectively disrupt mitochondrial membrane potential and inhibit electron transport chain function， leading to MQC dysfunction. Recent studies have confirmed that acupuncture can restore MQC homeostasis after IS through multiple targets and pathways， specifically including promoting mitochondrial biogenesis， balancing mitochondrial fission and fusion， regulating mitochondrial autophagy， reducing oxidative stress damage， and inhibiting calcium overload. This article systematically reviews the relationship between MQC and IS， with a focus on elucidating the mechanistic basis of acupuncture-mediated IS treatment via regulating key MQC components. These findings provide a theoretical basis for the efficacy of acupuncture in IS management and offer novel perspectives for developing future stroke therapeutic strategies targeting MQC pathways.

Lung transplantation （LTx） is the only effective curative treatment for end-stage lung disease （ESLD）， applicable to patients with advanced lung diseases who do not respond to medical and other surgical management， and can significantly improve the prognosis. However， LTx still faces many challenges， such as ischemia-reperfusion injury （IRI） and low long-term survival. Improving lung IRI is of great significance for the recovery of lung function and the prognosis of patients after transplantation. Lung IRI is a response to tissue damage and inflammation that worsens when the blood supply to the lung tissue is restored （reperfusion） after it has undergone a disruption of blood flow （ischemia）. IRI is an important pathophysiological basis for primary graft dysfunction （PGD）， and its injury mechanisms are complex and diverse， involving the activation of multiple cell deaths. Programmed cell death （PCD） is a highly ordered process of cell self-extinction regulated by genes， mainly including apoptosis， necroptosis， autophagy， ferroptosis， pyroptosis and cuproptosis， which are of great physiological significance for maintaining biological development， homeostasis and immune defense. Recent studies have shown that the activation of multiple PCDs is closely related to the occurrence and development of lung IRI. PCD is widely involved in lung IRI through different molecular mechanisms， but its specific regulatory mechanism has not been fully elucidated. This article systematically reviews the latest progress of various types of PCD in lung IRI， analyzes the molecular mechanism and interaction of PCD in lung IRI， and explores their potential as therapeutic targets， aiming to provide new insights for the development of clinical lung protection strategies.

Amyloid-β peptide （Aβ） is considered a major cause of Alzheimer's disease （AD）. However， current researches emphasize that Aβ can activate microglia and astrocytes， which causes neuroinflammation. Neuroinflammation plays a crucial role in the neuronal mortality process， and can be considered the underlying cause of AD. In addition， vascular damage was proposed to play an important role in the pathogenesis of AD more than two decades ago， but few researchers have focused on the positive role of cerebrovascular damage in AD. In recent years， a growing body of evidence has supported that brain microvascular injury causes the occurrence of AD. Moreover， recent research indicated that inflammation caused by brain microvascular injury is also a significant risk factor for the development of AD. In damaged microvessels， C-reactive protein （CRP） is a non-specific inflammatory marker， which can activate the complement and enhance phagocytosis of immune cells， and help to eliminate pathogenic microorganisms from the body. The plenty of evidence indicated that CRP penetrated brain tissue and participated in neuroinflammation during brain microvascular injury， thereby influencing the pathogenesis of AD. Therefore， the negative effects of CRP and Aβ on the pathogenesis of AD are equally important. At present， few researchers have established a link between the effects of CRP and Aβ on AD and conducted in-depth analysis. This article firstly and deeply analyzed and summarized the significant function and connection of Aβ and CRP in AD， which provided support for the theory that neuronal cerebrovascular injury is the cause of AD.

Cataract remains a cause of growing blind worldwide， and phacoemulsification is currently the preferred surgical technique due to its minimal invasiveness and rapid recovery. However， the intraoperative parameters setting of phacoemulsification remains crucial due to their potential impact on ocular tissues， particularly the corneal endothelium and retina. This review systematically examines the effects and interactions of these critical parameters during phacoemulsification， including ultrasonic frequency， infusion bottle height， and ultrasound energy. High-frequency ultrasound enhances emulsification efficiency and reduces operation time but significantly increases localized thermal effects， especially when combined with high-energy output， exacerbating the risk of thermal damage to the corneal endothelium. While a high bottle height stabilizes the anterior chamber， it simultaneously elevates mechanical shear stress and turbulence， further damaging endothelial cells. Conversely， low bottle height combined with low vacuum settings protects endothelial cells but may compromise chamber stability， increasing surgical difficulty. Additionally， oxidative stress and inflammatory cytokines， such as reactive oxygen species （ROS）， vascular endothelial growth factor（VEGF） and interleukin（IL）-6， significantly contribute to tissue injury， particularly pronounced in diabetic and ocular fundus disease patients. Based on current evidence， this article provides specific recommendations for parameter settings tailored to patients with hard nuclear cataracts， compromised corneal endothelial function， diabetes， and postoperative glaucoma. Moreover， this review highlights current research limitations， including high heterogeneity in clinical data， insufficient long-term follow-up， and inadequate mechanistic understanding. Future research should prioritize individualized parameter optimization， long-term clinical outcomes evaluation， and real-time intraoperative monitoring techniques， aiming to enhance surgical safety， reduce complications， and improve visual outcomes.

ObjectiveCardiovascular diseases pose a major public health challenge in China. The burden of cardiovascular disease associated with high low-density lipoprotein cholesterol （LDL-C） has increased steadily nationwide. A comprehensive analysis of secular trends in cardiovascular disease burden and its determinants is crucial for developing targeted interventions and evidence-based health policies. MethodsBased on data from the Global Burden of Disease Study 2021， we analyzed the trends in deaths， disability-adjusted life years （DALYs）， age-standardized mortality rates （ASMR）， and age-standardized DALY rates （ASDR） of cardiovascular diseases attributable to high LDL-C in China from 1990 to 2021 using Joinpoint regression analysis. An age-period-cohort model was applied to assess the contributions of age， period， and cohort effects to changes in the cardiovascular disease burden attributable to high LDL-C. Projections of the high LDL-C-attributable cardiovascular disease burden in China from 2022 to 2030 were generated using a Bayesian age-period-cohort model. ResultsBetween 1990 and 2021， China saw a substantial rise in both deaths and disability-adjusted life years （DALYs） from cardiovascular disease linked to high LDL-C. Joinpoint regression revealed key turning points in this trend： an overall increase continued until 2004， after which the burden began to fall starting in 2011. Throughout this period， age-standardized mortality and DALY rates were consistently higher in males than in females. Age-period-cohort analysis further indicated that mortality and DALY rates due to high LDL-C increased almost exponentially with age， while period and cohort risks generally decreased over time. Projections suggest a continued decline in age-standardized mortality rates from LDL-C-related cardiovascular disease for both Chinese men and women by 2030. ConclusionRapid population growth and accelerated ageing in China emerge as primary drivers of the escalating cardiovascular diseases burden linked to elevated LDL-C. The burden of cardiovascular diseases is higher in men compared to women. By 2030， the burden of cardiovascular disease caused by high LDL-C in China will remain severe. These findings underscore the critical need for gender-specific screening protocols， age-tailored interventions， and personalized management frameworks to mitigate this public health challenge.

ObjectiveTransfusion-Related Acute Lung Injury （TRALI） is a common fatal transfusion adverse reaction. Major Histocompatibility Complex （MHC） class I is an important factor involved in the pathogenesis of TRALI； however， the role of complement in itspathogenesis has not been fully elucidated. This study aims to explore the role of complement in MHC class I antibody-mediated TRALI， so as to provide a theoretical basis for clinical prevention and treatment. MethodsThis study established a murine model of transfusion-related acute lung injury （TRALI） based on the "two-hit" theory， with lipopolysaccharide （LPS） as the first hit and MHC class I antibody as the second hit. Male Balb/c mice were randomly divided into seven groups （n=5 per group per experiment）： Naive （blank control）， LPS （first hit only）， Isotype （isotype antibody control）， TRALI （model group）， C5aR1 inhi （C5aR1 antagonist intervention）， C5aR2 inhi （C5aR2 antagonist intervention）， and Anti-C5 （anti-complement C5 antibody intervention）. Rectal temperature was monitored after MHC class I antibody injection. After sample collection， the severity of pulmonary edema was assessed by measuring the lung wet-to-dry weight ratio， histological analysis， and immunohistochemistry. Serum and bronchoalveolar lavage fluid were collected to measure cytokine and complement levels. ResultsMice in the TRALI group exhibited a significant decrease in rectal temperature， an increased lung wet-to-dry weight ratio， elevated serum cytokine levels， and markedly heightened complement C5a levels in bronchoalveolar lavage fluid （P＜0.000 1）. Histopathological examination revealed substantial infiltration of inflammatory cells， predominantly neutrophils accompanied by fewer lymphocytes， plasma cells， and monocytes， along with increased deposition of the membrane attack complex C5b-9 in lung tissues. In contrast， mice treated with anti-C5 antibody demonstrated no significant decrease in rectal temperature. The lung wet-to-dry weight ratio in this group showed no statistical difference compared to either the Naive or Isotype control groups （P＞0.05）. Furthermore， these mice displayed reduced serum cytokine levels， a significant attenuation of inflammatory cell infiltration in the lungs， and a 100% survival rate at the 2-hour time point. However， mice administered either the C5aR1 antagonist or the C5aR2 antagonist failed to be protected and subsequently developed TRALI. ConclusionComplement activation， which forms the membrane attack complex C5b-9， plays a critical role in MHC class I antibody-mediated TRALI. Blocking complement C5 activation can effectively prevent the occurrence of TRALI.